I can't find much information about this substance or well...mixture. Anyone have any experience of knowledge of it.

I'm trying to lower my amphetamine tolerance and I have a decent amount of methylphenidate, but honestly I feel disgusting when using it.
a dose of 50-60mg gives me jitters, chest pain but on the left side, not exactly heart pain, and makes me feel really sketchy or it gives me moderate stimulation and focus briefly then jitters and shakyness. either way it feels like crap. If I were to mix ethanol into this combo and lower the ritalin dosage, would it possibly be less of a terrible shaky high and perhaps somewhat enjoyable/smooth. I can do up to 90mg amp and get no jitters, worst side effect is vasoconstriction.

This is not a good idea--the combination of EtOH and methylphenidate will end up doing more cardiac damage than MPH alone and the in vivo formation of d-ethylphenidate is pretty limited (a lot more inactive l-enantiomer is formed). Honestly, this is why I switched from MPH to dexamphetamine: MPH just starts to feel peripherally nasty after you've been on it for a while, with jitteriness, yet central tiredness and a rollercoaster up and down effect. With 45-60mg dexamphetamine XR per day, I've never experienced rising tolerance, any significant crash/comedown or typically reported nasties (jitters, anorectic effect, anxiety/insomnia).

well, if it d/l methylphenidate is consumed (Orally or insufflated) and then alcohol (Lets say vodka)

I have plenty of amp, but I really am trying to lower the amount I use. I figured some other dopamine acting drug would be useful, and I happen to have about 150mg of ritalin to waste. I hate alcohol and depressants in general and am supposed to go out to a club tonight. So ethylphenidate has higher cardiac damage potential? The things i've read about it say it has no added toxicity which is why it seemed appealing but if thats true i already notice the peripherals from this shit are aweful so I dunno. The few reports I've seen all point towards its negatives being muted by the alcohol. I'm referring moreso to metabolizing ritalin + alc than if its possible to create ethylphenidate out of ritalin as a salt. Im not really sure. A bit mentally foggy today..

So by how would I go about dosing with alcohol/mph
drink some vodka, take a few, then a bit more to drink?
I don't like drinking/drink alot so I only want enough to get the effects of ethylphenidate
And if this worsens the crash I have k-pins for backup

I don't usually do mph in any form, and I find regular mph to be kinda like a cracked out version of caffeine. Snorting it brought a LITTLE euphoria a while ago, but I rarely ever use it. My girlfriend has about 240 10mg pills though, she rarely takes her script, and she said since I wan't to stop using so much amphetamine I can have a bunch of her ritalin.

I agree though about racemic mph, it definately feels completely peripheral, the only cns effect is a zombie-like dulled out state...

I was hoping ethyl may be a bit more euphoric party oriented stimulation than a twitching zombie state

Ham, I'm not sure if enzymes DO target isomers selectively, but the concept doesn't seem implausible to me, we are after all, made up of proteins, including the enzymes, and made up of amino acids, all having a chiral center (save for glycine of course)

I see no reason why having a different chirality couldn't affect the ability of a ligand to dock in the active site of an enzyme, it does with receptors for neurotransmitters.

IIRC thalidomide is interconverted in vivo, one isomer is teratogenic and one isn't, but metabolically the two are interconverted (hepatic metabolism I think, enzymatic), administer the nontoxic isomer, and the toxic one will be created in vivo.

IIRC thalidomide is interconverted in vivo, one isomer is teratogenic and one isn't, but metabolically the two are interconverted (hepatic metabolism I think, enzymatic), administer the nontoxic isomer, and the toxic one will be created in vivo.

Ham, I'm not sure if enzymes DO target isomers selectively, but the concept doesn't seem implausible to me, we are after all, made up of proteins, including the enzymes, and made up of amino acids, all having a chiral center (save for glycine of course)

I see no reason why having a different chirality couldn't affect the ability of a ligand to dock in the active site of an enzyme, it does with receptors for neurotransmitters.

IIRC thalidomide is interconverted in vivo, one isomer is teratogenic and one isn't, but metabolically the two are interconverted (hepatic metabolism I think, enzymatic), administer the nontoxic isomer, and the toxic one will be created in vivo.

Right, it's certainly possible, but I've never heard of it being true here. I'd be a bit surprised, were enzymes metabolizing isomers preferentially one isomer would have a longer activity in the body. That's true for some things, but AFAICT, not for MPH.

This is a different enzyme, but for our liver, enzymes that target both equally is an advantage, but for our brains, being selective is an imperative (especially between DA and NE/E receptors)